ICS Flashcards
What cells predominate in acute inflammation?
Neutrophil polymorphs.
What cells predominate in chronic inflammation?
Lymphocytes, plasma cells + macrophages.
Briefly explain the process of acute inflammation.
- Initial reaction of tissue to injury.
- Vascular component – vasodilation.
- Exudative component (vascular leakage of protein-rich fluid).
- Neutrophil polymorph recruitment to tissue.
What are the cardinal features of inflammation?
- Redness (rubor).
- Het (calor).
- Swelling (tumor).
- Pain (dolor).
- Loss of function.
What are the potential outcomes of inflammation?
- Resolution.
- Suppuration = pus formaiton.
- Organisation = repair of specialised tissues by formation of fibrous scar.
- Chronic inflammation > fibrosis.
What is a granuloma?
Aggregate of epithelioid histiocytes.
What is granulation tissue?
New connective tissue + small blood vessels that form on surface of a wound.
What is the different between resolution and repair in inflammation?
- Resolution occurs when initiating factor is removed + tissue is either undamaged or able to regenerate.
- Repair occurs when initiating factor is still present but tissue is damaged/unable to regenerate, involves replacement of damaged tissue by fibrous tissue.
What cells are capable of regeneration?
- Hepatocytes.
- Pneumocytes.
- Gut + skin epithelial cells.
- All blood cells.
- Osteocytes.
What cells are incapable of regeneration?
- Neurones.
- Myocardial cells.
Define and give an example of…
i) Apoptosis.
ii) Necrosis.
iii) Atrophy.
i) Programmed cell death as a result of stimuli, too much = HIV, not enough = cancer.
ii) Traumatic cell death, occurs due to infarction like MI, CVA, frostbite.
iii) Decrease in the size of a tissue caused by a decrease in the number of constituent cells/decrease in their size, seen in Alzheimer’s disease.
Define and give an example of…
i) Hypertrophy.
ii) Hyperplasia.
iii) Metaplasia.
i) Increase in size of a tissue caused by an increase in size of constituent cells, building muscle.
ii) Increase in size of a tissue caused by an increase in the number of constituent cells, prostatic hyperplasia.
iii) Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type, Barrett’s oesophagus.
Define.
i) Dysplasia.
ii) Neoplasia
i) Morphological changes seen in cells progressing to cancer.
ii) New + abnormal growth of tissue in the body which persists despite removal of initial stimulus.
What is a tumour? What’s the difference between benign + malignant neoplasms?
- Any abnormal swelling.
- Benign = localised, slow growth rate, low mitotic activity.
- Malignant = invasive, metastases, rapid growth rate.
What are the two types of benign epithelial neoplasms?
- Papilloma = benign tumour of non-glandular, non-secretory epithelium.
- Adenoma = benign tumour of glandular or secretory epithelium.
What are the two types of malignant epithelial neoplasms?
- Carcinoma = malignant epithelial neoplasm.
- Adenocarcinoma = carcinoma of glandular epithelium.
How are benign connective tissue neoplasms named?
Suffix -oma…
- Rhabdomyoma (striated muscle)
- Leiomyoma (smooth muscle).
How are malignant connective tissue neoplasms named?
Suffix -sarcoma…
- Liposarcoma = adipose tissue.
- Angiosarcoma = blood vessels.
What is carcinogenesis?
- Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations.
What type of cancers are caused by…
i) Polycyclic aromatic hydrocarbons (smoking, mineral oils).
ii) Aromatic amines (rubber/dye workers)
iii) Nitrosamines.
iv) Alkylating agents.
i) Lung, skin.
ii) Bladder.
iii) Gut.
iv) Leukaemia.
How can tumours spread?
- Invades basement membrane using collagenases
- Tumour motility.
- Enters lymph/blood vessels.
- Evades host immune defence.
- Triggers angiogenesis to nurture growth at new site.
What is the likely origin of…
i) Lung metastases?
ii) Liver metastases?
iii) Bone metastases?
i) Sarcomas, many common (breast).
ii) Colorectal, stomach, pancreas, carcinoid of intestine.
iii) Prostate, breast, thyroid, lung + kidney.
What is innate immunity?
- Non-specific, instinctive, present from birth + first line of defence.
Name some components of the innate immune system.
Physical + chemical barriers…
- Mucous in resp tract, skin as physical barrier, low vaginal pH, acidic gut.
Phagocytic cells like neutrophils + macrophages.
Serum proteins like complement, acute phase proteins.
What ways can complement activation occur?
Classical pathway... - Antibody-antigen immune complexes. Alternative pathway... - Foreign surfaces-antigens. Lectin pathway... - Mannose-binding lectin, mannose residues on pathogen surface.
What is the complement pathway?
- Lyse microbes directly (formation of membrane attack complex).
- Increase chemotaxis, cell recruitment (C3a + C5a).
- Opsonisation (increasing phagocytosis, C3b).
What is adaptive immunity?
- Specific, requires lymphocytes, memory + quicker response.
What is the major histocompatibility complex? What are the two classes?
Proteins that mark a cell as SELF.
Class I = all nucleated cells (not RBCs)
- E.g. virus infected or cancer cell.
Class II = certain immune cells, antigen-presenting.
- E.g. macrophages, B cells, dendritic cells.
What are pattern recognition receptors?
- Secreted + circulating like lectins and collectins.
- Cell associated like toll/nod-like receptors.
What are the things are recognised in relation to pattern recognition receptors?
- Pathogen associated molecular patterns (PAMPs) like lipopolysaccharides.
- Damage associated molecular patterns (DAMPs).
Where are T lymphocytes produced + matured? How do T cells recognise antigens?
- Produced in bone marrow, mature in thymus.
- Must be displayed by an antigen presenting cell bound to MHC1/2.
What are the two types of T cells?
Cytotoxic T cells (CD8)…
- Destroy infected body cells (apoptosis) by binding to antigens.
- Binds to MHCI.
T helper cells (CD4)…
- Binds to MHCII.
- Th1 secretes cytokines.
- Th2 activates eosinophils, basophils, induce B cells to make antibodies by releasing cytokines to induce B-cell proliferation.
Where are B lymphocytes produced + matured? What do they do? How are they activated?
- Produced + mature in bone marrow.
- Recognise soluble, free, native, polypeptide antigens.
- Travel to lymph nodes where they proliferate + differentiate into plasma cells (secrete antibodies) + memory B cells (immunity).
What are the functions of antibodies?
- Neutralise toxins.
- Opsonisation.
- Activate classical complement system.
What are the different types of antibodies?
- IgM = made first.
- IgG = most common, crosses placenta (passive immunity).
- IgA = secreted from mucous membranes (breast milk).
- IgD = B cella ctivation.
- IgE = histamine reactions + allergies.
What is the Fab and Fc region of antibodies?
- Fab region is part that binds to epitope of an antigen.
- Fc region is part that binds to B cells.
What does specific binding of the Fab region lead to?
- Neutralise toxins (IgG, A).
- Immobilise motile microbes (IgM).
- Prevent binding to + infection of host cells.
What are the enhance innate mechanisms with the Fc region?
- Activate complement (IgG, M).
Bind Fc receptors… - Phagocytes (IgG, A) enhances phagocytosis.
- Mast cells (IgE) release inflammatory mediators.
- Natural killer cells (IgG) enhanced killing of infected cells.
What is hypersensitivity?
- The immune system responds inappropriately to a normal harmless antigen.
What is a type 1 hypersensitivity reaction
- IgE mediated, allergic + acute.
- IgE binds to mast cells causing histamine release.
- Anaphylaxis, hayfever.
What is a type 2 hypersensitivity reaction
- IgG bound to cell surface antigens/IgM
- Transfusion reactions, autoimmune disease, goodpastures.
What is a type 3 hypersensitivity reaction
Immune complexes, activation of complement/IgG.
- SLE.
What is a type 4 hypersensitivity reaction
T-cell mediated delayed type hypersensitivity.
- TB, contact dermatitis.
Briefly describe immunity.
First exposure…
- IgM made first, rapidly increases.
- IgG begins to be made, rapidly increase.
- IgM decreases first, IgG decreases after.
Second exposure…
- IgG RAPIDLY produced in vast quantities.
- Small rise in IgM.
- Symptoms not experienced second exposure.
What is the aim of vaccinations?
- Achieve long-term protection, stimulate both B+T cells, induce memory B+T cells + stimulate protective high affinity IgG production.
